The Status of Serum Lipid Profile in Stress-Related Pre-insomnia

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Uba A.I et al. European Journal of Biomedical and Pharmaceutical Sciences

THE STATUS OF SERUM LIPID PROFILE IN STRESS-RELATED

PRE-INSOMNIA

Uba A.I1,2

*, Abdullahi I.L2, Abdullahi, S.A

2 and Adamu H

2

1Department of Biochemistry, Bayero University, Kano, P.M.B 3011, Kano-Nigeria

2Centre for Biotechnology Research, Bayero University, Kano P.M.B 3011, Kano-Nigeria

Article Received on 03/12/2014 Article Revised on 24/12/2014 Article Accepted on 15/01/2015

ABSTRACT

Understanding of the correlation between stress, pre-insomnia and

serum lipid profile status may provide clues toward the management of

stress- related cardiovascular diseases. This study assessed the serum

lipid profile on a total of thirty seven (37) male and female subjects;

twenty eight (28) of which are students selected from different

departments and nine (9), within Kano city. Twenty five (25) served as experimental

subjects and twelve (12) as control subjects. Their blood pressure was taken and

information on general life style, sleeping as well as reading habits was recorded by means of

well-structured questionnaire prior to sample collection. Venous blood (5ml) was collected

from each subject, centrifuged and the sera stored. Serum lipid profile was assayed using

commercial kit from fortress diagnostics limited. When the Mean serum Total Cholesterol,

High Density Lipoprotein Cholesterol, Low Density Lipoprotein Cholesterol and Triglyceride

levels of test subjects were compared with those of the control subjects the difference was not

significant (p˃0.05). When comparison was made within the study group, based on

borderline risk of high and normal blood pressure, the serum lipid profile level was found to

differ significantly (p˂0.05). Thus our study showed that acute sleep deprivation (pre-

insomnia) does not alter serum lipid profile, however, is associated with mild hypertension

which is a risk factor for cardiovascular diseases.

KEYWORDS: Pre-insomnia, Stress, Lipid profile.

European Journal of Biomedical AND

Pharmaceutical sciences http://www.ejbps.com

ISSN 2349-8870

Volume: 2

Issue: 1

89-98

Year: 2015

Research Article ejbps, 2015, Volume 2, Issue 1, 89-98.

*Correspondence for

Author

Uba A.I PhD (In view)

Department of Biochemistry,

Bayero University, Kano,

P.M.B 3011, Kano-Nigeria.

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1.1 INTRODUCTION

Insomnia is a subjective feeling of having difficulty initiating, maintaining or restoring sleep,

or having poor sleep quality (Roth, 2007). It was reported to be associated with substantial

impairments of an individual’s quality of life (Leger et al., 2012), depression (Sarsour, et al.,

2010) and accident occurrence (Chiang, et al., 2012). Insomnia is the most common sleep

disorder, affecting one in four people (Kessler 2011; Shatzmiller 2012; American Academy

of sleep medicine 2001). Many people may not realize that insomnia and short sleep duration

correlate with various health problems including cardiovascular disease, anxiety, and

potentially cancer (Terauchi 2012; Chayon 1998; Kakizaki 2008; Verkasalo 2005; Philips

2007). Insomnia also increases mortality in adults (Chien, 2010 and Hublin 2011). Although

the cause and physiology of insomnia have not been completely understood, it is generally

considered as one kind of hyperarousal disorder related to increased activity of hypothalamic

pituitary adrenal-axis (Roth, 2007). During this process cortisol (Vgontzas et al.,2001) will be

secreted excessively. Elevated cortisol is able to induce higher cholesterol (Fraser et al.,

1999).

Pre-insomnia (onset of insomnia) may be a consequence of another underlying medical

problem e.g. mental health issue, physical health issue, hormonal imbalance, medication, and

stimulant. Recently, it was demonstrated that paradoxical sleep deprivation for four days has

significant effect on lipid metabolism such as increasing Low Density Lipoproteins

(Anderson et al.,2004). In addition, cholesterol concentration was significantly decreased in

rats exposed to cold environmental temperatures, indicating increase corticosterone synthesis

and activation of HPA system (Cvijic, Davidovic and Jordjevic, 2003). Recent study

suggested that short sleep duration was associated with higher risks of hypercholesterolaemia

in the adults of U.S (Gangswisch et al.,2010) and japan (Kaneita et al, 2008) likewise reduce

sleep duration was found to be related to dyslipidemia in other studies (Chen, and Zhang,

2014).

During the past two decades, considerable evidence has accumulated showing an association

between cardiovascular disease (especially adverse coronary artery disease) and markers of

stress and other psychological factors, such as anxiety, depression and somatization (Artham

et al., 2008; Hemingway and Marmot, 1999; Rozansk et al.,2005). Recent studies have

shown that disturbed sleep and sleep deprivation are associated with subsequent occurrence

of cardiovascular alterations (Stickgold and Walker, 2007; Cintra et al.,2005; Perry et

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al.,2007), behavoural changes (Anderson et al., 2005; Spiegel, Sheridan, and Van Cauter,

2002; Andersen et al., 2006) as a result of weight loss; however, unlike the decrease in LDL,

the reduction of triglyceride concentration is not related to this weight reduction (Perry et

al.,2007). Another ones have shown that habitual sleep duration <5hr per night is associated

with an increased prevalence of arterial hypertension (Gangwischet al., 2006; Gottlieb et

al.,2006; Cappuccio et al.,2007). Some articles have proposed that activation of the

sympathetic nervous system by sleep deprivation may be involved in triggering

cardiovascular events in the morning hours (Tochikubo et al., 1996 and Lusardi et al., 1999).

A review reported by Dimsdale and Herd showed that the level of free fatty acids and total

cholesterol increases in acute and chronic stress (Dimsdale, 1982), which may be attributed to

insomnic condition. Similarly a study conducted by Fakhari and colleagues in 2004

demonstrated increased triglyceride in individuals who had experienced high levels of stress

in the preceding 6-12 months (Fakhari et al.,2007). This may be attributed to the finding that

cortisol causes the mobilization of fats (lipids) deposited in the adipose and other tissues,

leading to an increased levels of lipids in the blood (Bower and Sergerstrom, 2001). More

recently, our previous work on stress has shown that the higher the examination stress the

higher the serum Cholesterol, Low Density Lipoprotein Cholesterol and Triglycerides levels

and lower the serum High Density Lipoprotein levels, suggesting an increased risk of

hyperlipidaemia in stress condition (Uba et al.,2014). The response to examination stress may

be related to the enhanced utilisation of cholesterol in the andrenal cortex for steriodogenesis

(Bijlani et al., 1986). Increase catecholamine levels result in up regulation of lipoprotein

lipase, leading to increased concentrations of free fatty acids(FFA) in the serum that are

transformed by the liver into cholesterol and triglycerides. Cortisol,on the other hand,

increases the deposition of abdorminal fat, which is more sensitive to lipolitic agents and

related to insulin resistance (Resmond, 2005), elevated lipid profiles in turn may mediate

longer term deleterious effects on physical health including heart disease and stroke.

The studies cited above have not been able establish proper correlation between stress, pre-

insomnia, lipid profile and cardiovascular disease. This study is aimed at determining serum

lipid profile status in pre-insomnic individuals in stress condition. The specific objectives are

(1) To find if pre-insomnic condition is enough to cause lipid profile alteration (2) To observe

whether an acute insomnia (pre-insomnia) is the risk factor for or the consequence of lipid

profile alteration..

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2.1 MATERIAL AND METHOD

2.1.1 Study Site, Subjects and Sample Collection

The study was carried out at Bayero University, Kano, Department of Biochemistry. A total

of thirty seven (37) male and female subjects; twenty eight (28) of which are students

selected from different departments and nine (9), within Kano city. Twenty five (25) served

as experimental subjects and 12 as control subjects.Their blood pressure was taken and

information on their general life style, including dietary habit was recorded by of means of

structured questionnaire prior to sample collection. Venous blood (5ml) was collected from

each subject, centrifuged and the sera stored.

The study was approved by the ethical committee of the institution and the informed consent

was obtained from the study subjects.

2.1.2 Methodology

2.1.2.1Estimation of Serum Lipid Profile

Serum total cholesterol was assayed by Tindar’s reaction (Evans and Stein, 1986; NIH,

1990), Serum Triglyceride level was determined as described by Fossati and Precipe (1982),

HDL-C, using commercial kit from fortress diagnostics limited and the serum LDC-L level

was calculated by Friedwald’s formular (Friedwald et al., 1972).

2.1.3 Statistical analysis

The result were expressed as means ± standard deviation. One – way analysis of variance

ANOVA was used to analyse Lipid Profile data followed by Student T-Test to calculate

statistical significance difference between the various groups.

The study was approved by the ethical committee of the institution and the informed consent

of the study subjects was obtained prior to experimentation.

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3.0 RESULT AND DISCUSSION

3.1 RESULT

Table 3.1: Mean ± standard deviation of serum total cholesterol, HDL-cholesterol, LDL-

Cholesterol, and Triglyceride

TC (mmol/l) TAG (mmol/l) HDL (mmol/l) LDL (mmol/l)

(Mean ± standard deviation)

Study subject

n = 25

3.14 ± 0.82 1.27 ± 0.37 1.27 ± 0.14 1.30 ± 0.63

(Mean ± Standard deviation)

control subject

n = 12

3.08 ± 0.80 1.12 ± 0.44 1.32 ± 0.13 1.21 ± 0.68

Values are mean ± standard deviation

When the mean serum Total Cholesterol, High Density Lipoprotein Cholesterol, Low Density

Lipoprotein Cholesterol and Triglyceride levels of test subjects were compared with those of

the control subjects the difference was not significant (p˃0.05)-(Table 4.1).

When comparison was done within the study group, based on high and normal blood

pressure, the mean serum lipid profile level was found to differ significantly with hgher mean

value from high blood pressure group (p˂0.05)-(Table 3.2).

Table 3.2: Mean ± standard deviation of TC, TG, HDL and LDL among the test

subjects with borderline risk of high blood pressure and normal blood pressure.

Test Subject TC (mmol/l) TAG (mmol/l) HDL

(mmol/l) LDL (mmol/l)

borderline risk of

high blood pressure 3.74 ± 0.85

a 1.44 ± 0.49

b 1.20 ± 0.07 1.76 ± 0.91

c

Normal blood

pressure 2.0 ± 0.21

a 0.95 ± 0.29

b 1.35 ± 0.12 0.37 ± 0.21

c

Values are mean ± standard deviation. Values with similar superscript are significant

(p˂0.05)

3.2 DISCUSSION

When the mean serum Total Cholesterol, High Density Lipoprotein Cholesterol, Low Density

Lipoprotein Cholesterol and Triglyceride levels of test subjects were compared with those of

the control subjects the difference was not significant (p˃0.05)-(Table 3.1). This result is

consistent with the findings of previous studies on the relationship between sub-acute or

acute sleep deprivation on lipid profile which reported that difficulty falling asleep was not

associated with TG or HDL-cholesterol (Troxel et al., 2010). Similarly, a review showed that

sleep deprivation does not change total cholesterol levels in rat (Anderson, 2009). Cholesterol

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level and Low Density Lipoprotein Cholesterol had no significant change in sub-chronic

sleep deprivation (Perry et al., 2007). Research showed that there is no significant changing

in cholesterol level in sleep deprived male rats (Antunes, 2007). A study on the effect of sleep

deprivation on 18 – 65 years old men and women, proved that short sleep deprivation had no

effect on total cholesterol levels (Adamkova, 2009). Thus acute sleep deprivation may be due

to acute effect of cardiovascular physiology arising from changes in the autonomic nervous

system, rather than Lipid profile (Artham et al., 2008).

However, our study is inconsistent with a report by Dimsdale and Herd that, the level of free

fatty acids and total cholesterol increases in chronic stress (Dimsdale and Herd, 1982), which

may be attributed to insomnia. Similarly a study conducted by Fakhari and colleagues in

2004 demonstrated increased triglyceride in individuals who had experienced high levels of

stress in the preceding 6-12 months (Fakhari et al.,2007). A very recent study has shown that

the higher the examination stress the higher the serum Cholesterol, Low Density Lipoprotein

Cholesterol and Triglycerides levels and lower the serum High Density Lipoprotein levels,

suggesting an increased risk of hyperlipidaemia in stress condition (Uba et al.,2014).

However, these reports evaluated effects of chronic sleep deprivation rather than acute or

sub-acute sleep deprivation (Pre-insomnia) being reported by our study.

Upon comparison within experimental subjects with borderline risk high blood pressure and

normal blood pressure groups, a significant increase (p˂0.05)-(Table 3.2) in total cholesterol,

triglyceride, low density lipoprotein cholesterol and a decrease (p˂0.05)-(Table 3.2) in high

density lipoprotein cholesterol levels in individuals with borderline risk of high blood

pressure was observed compared with normal blood pressure individuals, suggesting that

acute insomnia is associated with prevalence of arterial hypertension. The individuals with

border line risk of high blood pressure were thought to be more stressed compared to those

with normal blood pressure, indicating an increase in electroencephalogram beta wave

activity of the brain, making it harder for the brain to achieve the state of relaxation needed

for sleep ( the brain still remain alert ). The body circadian rhythm and time may be

disconnected, resulting in disruption of normal sleeping pattern.

Cortisol is a stress hormone secreted at higher level during stress for appropriate stress

response. Although the secretion may not be so significant to cause a vast alteration in pre-

insomnic individuals, these subjects tend to have an increased blood sugar level thought to

be produced by gluconeogenesis through the activation of pyruvate carboxylase, an enzyme

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that generate oxaloacetate, an important precursor of glucose in the pathway. The glucose

produced provides energy to the brain. This high glucose metabolism leads to the inability of

the brain to get full relaxation even during sleep. (Uba et al.,2014). The pre-insomnic

condition can thus be attributed to stress as far as our study subjects are concerned.

3.3 CONCLUSION

Our study shows that acute sleep deprivation (pre-insumnia) does not alter serum TC, TG,

HDL and LDL cholesterol significantly, however, in stress condition borderline of high blood

pressure subjects showed low risk of developing cardiovascular diseases.

4.4 RECOMMENDATION

We recommend further research to investigate cardiac enzymes, blood glucose, cerebrospinal

fluid levels of individuals with chronic insomnia.

4.5 ACKNOWLEDGEMENT

We acknowledge the technical assistance of the laboratory technicians, Department of

Biochemistry, Bayero University, Kano and S.S Usman for critical reading of the manuscript

and making suggestions.

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The Status of Serum Lipid Profile in Stress-Related Pre-insomnia

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